Beta-amyloid peptide (Abeta), the major constituent of amyloid plaques in the
brains of Alzheimerâ��s patients, is thought to be the cause of Alzheimerâ��s Disease
(AD). Alzheimerâ��s diseased brains show significant levels of Abeta (11-40) and
Abeta (11-42). The Ã�-secretase enzyme or Ã�- amyloid precursor protein-cleaving
enzyme (BACE) generates the N terminus of AÃ�, producing full-length Abeta (1-
40 and 1-42) and/or truncated Abeta (11-40 and 11-42). The abundance of Abeta
(11-40 and 11-42) produced by BACE suggests that they might be playing an
important role in Alzheimerâ��s disease pathogenesis.